pulmonary blood flow, gas exchange and transport Flashcards
describe the blood supply to the lungs
pulmonary artery
pulmonary vein
what is the role of the pulmonary artery
travels away from the heart carries blood to the lungs L and R arise from R ventricle carries entire cardiac output from RV supplies the dense capillary network surrounding the alveoli
pulmonary vein
travels into the heart
returns oxy blood to the LA
how is pulmonary circulation different to systemic circulation
opposite in function - delivers carbon dioxide to the lungs and picks up oxygen
high flow, low pressure system (systolic ~25mmHg)
bronchial circulation
supplied by the bronchial arteries arising from the systemic circulation
supply oxygenated blood to the airway smooth muscle, nerves and lung tissue (lung parenchyma)
remove waste
comes from the L side of the heart
describe the factors that influence diffusion of gases across the alveoli
obey the rules for siple diffusion
rate of diffusion across the membrane is:
directly proportional to pp grad
directly proportional to gas solubility
directly proportional to available SA
inversely proportional to thickness of the membrane
most rapid over short distances
pressure gradients for oxygen and carbon dioxide between alveoli and pulmonary arterial blood
OXYGEN: 100mmHg in alveoli –> 40mmHg in arterial blood
CARBON DIOXIDE: 46mmHg in arterial blood –> 40mmHg in alveoli
what is arterial blood pp equivalent to
alveoli
what is venous blood pp equivalent to
tissue
partial pressure of oxygen and carbon dioxide in tissues
oxygen: <40
carbon dioxide: >46
what is rate affected by
solubility of the molecule
oxygen isn’t very soluble in water but carbon dioxide is
how are the alveoli adapted for efficient diffusion
large SA
short diffusion distance
membranes are thin
elastic fibres and type II cells never sit between the capillary and the type I cell
impact of emphysema on gas exchange in the lung
destruction of the alveoli
reduced SA for gas exchange
low pO2 in the blood
normal alveolar PO2
impact of fibrosis on gas exchange
thickened alveolar membrane slows gas exchange
loss of lung compliance may decrease alveolar ventilation
normal or low alveolar PO2
low blood PO2
impact of pulmonary oedema on gas exchange
fluid in the interstitial space increases diffusion distance
arterial PCO2 may be normal due to higher solubility of CO2 in water
normal alveolar PO2
low PO2 in blood
impact of asthma on gas exchange
constricted bronchioles
increased airway resistance
decreased airway ventilation
low alveolar and blood PO2
explain the relationship between ventilation and perfusion and its significance in health
ventilation and perfusion ideally compliment each other
optimally, ventilation = blood flow
both blood flow and ventilation decrease with height across the lung
describe the V/Q relationship at the base of the lungs
V
describe the V/Q relationship at the apex of the lungs
low blood flow
arterial pressure < alveolar pressure
arteries are compressed
what % of the height of the healthy lung performs well in matching blood and air
75
the majority of the mismatch occurs in the apex
this is then auto-regulated to keep the ratio close to 1
what happens when ventilation decresaes in a group of alveoli
PCO2 increases
PO2 decreases
blood flowing past these alveoli isnt oxygenated
dilution of blood from better ventilated areas
describe the local control mechanisms that keep ventilation and perfusion matched
decreased PO2 around under ventilated alveoli constricts their arterioles, diverting blood to better ventilated alveoli
increased PCO2 causes mild bronchodilation
constriction in response to hypoxia is particular to pulmonary vessels
what occurs when ventilation > blood flow
alveolar dead space
air in the alveoli isn’t participating in gas exchange due to insufficient blood flow
what occurs with alveolar dead space
opposite to shunt
increased alveolar PO2 - pulmonary vasodilation
decreased alveolar PCO2 - mild bronchial constriction
this increases perfusion and decreases ventilation, bringing the ratio back towards 1
define shunt
the passage of blood through areas of the lung that are poorly ventilated
opposite of alveolar dead space
define anatomical dead space
air in the conducting zone of the resp tract unable to participate in gas exchange as walls of airway in this region are too thick
physiologic dead space
alveolar DS + anatomical dead space
dalton’s law
total pressure of a gas mixture is the sum of the pressures of the individual gases
henry’s law
amount of gas dissolved in a liquid is determined by the pressure of the gas and its solubility in the liquid
define partial pressure
the pressure of a gas in a mixture of gases is equivalent to the % of that particular gas in the entire mixture multiplied by the pressure of the whole gaseous mixture
how many ml of oxygen dissolve per L of plasma
3ml
how does Hb in RBC influence the carrying capacity
increases it to 200ml/L
>98% bound to Hb, the rest is in the plasma
Hb is required to meet the oxygen demand of resting tissues
what is the difference between arterial partial pressure of oxygen and arterial oxygen content
arterial pp of oxygen is not the same as arterial oxygen concentration/content
PaO2 refers to oxygen in solution in the plasma and is determined by oxygen solubility and pp of O2 in the gas phase
what are the value assigned to pp of a gas in solution equal to
the pp of the gaseous phase that is driving that gas into solution
REMEMBER THAT GASES DONT TRAVEL IN THE GASEOUS PHASE IN THE PLASMA
what is PaO2
100mmHg
same as in alveoli
aka oxygen tension
how much of arterial oxygen is extracted by the peripheral tissues at rest
25%
how does Hb bind to oxygen
cooperatively binds 4 molecules of O2
1.34ml O2 to 1g Hb
HbA
92% of the Hb in RBC is HbA, the remaining 8% is HbA2 (delta chains replace beta), HbF (gamma replace beta) and glycosylated Hb (HbA1A, HbA1B, HbA1C)
how is glycosylated Hb related to diabetes
if BG levels increase, glycosylation of Hb increases
indicative of diabetes management over time
glycosylation is permanent for the lifetime of that RBC
what is the major determinant to the degree of % O2 saturation
PaO2
Hb and oxygen transport
Hb sequesters O2 from the plasma
pp gradient is maintained until the Hb is saturated w/ O2
How long does saturation of Hb w/ O2 take
complete after 0.25s contact w/ the alveoli
total contact time ~0.75s
O2 Hb dissociation curve
shows PO2 (mmHg) against Hb % saturation O2 sigmoidal shaped max saturation = 98%
when is Hb most saturated
at normal systemic PaO2
100mmHg
even at 60mmHg, Hb is still 90% saturated
at normal venous PO2 there is still 75% reserve capacity
what happens to saturation below 40mmHg
small changes in PO2 create much larger changes in % saturation
factors affecting the O2 - Hb dissociation curve
ph
PCO2
temp
2,3-DPG
Effect of Ph on the O2 - Hb dissociation curve
reduced pH (acidosis) - curve shifts right increased pH (alkalosis) - curve shifts left
effect of PCO2 on the O2 - Hb dissociation curve
increased pp shifts the curve right
effect of temp on the O2 - Hb dissociation curve
increase temp shifts the curve right - lower affinity for oxygen at higher temps, oxygen given off more readily to the peripheral tissues, low % bound to Hb
hypothermia - curve shifts L, Hb doesn’t release oxygen to peripheral tissues, high affinity
effect of 2,3 DPG on the O2 - Hb dissociation curve
synthesised by RBC
increases in situations associated w/ inadequate oxygen supply and helps maintain oxygen release in the tissues
affinity of Hb for O2 is reduced by the binding of 2,3 - DPG
foetal Hb and myoglobin compared to normal adult Hb
both have a higher affinity for oxygen than HbA - this is necessary for extracting oxygen from maternal/arterial blood (muscle requirers high amounts of oxygen delivery)
at any pp they have a higher % sat than HbA
what is anaemia
any condition where the oxygen carrying capacity of the blood is compromised
NO CHANGE IN PaO2 (only RBC are affected)
total blood content is reduced as most O2 is associated w/ RBC
Hb present is still fully saturated as PaO2 is normal
what are 3 causes of anaemia
iron deficiency
vit B12 deficiency
haemorrhage
what does carbon monoxide bind to in the blood
Hb forming carboxyhaemoglobin
250x greater affinity than O2
only a small PCO is needed for progressive carboxyHb formation
symptoms of CO poisoning
hypoxia and aneamia nausea and headaches cherry red skin and mucous membranes normal resp rate (normal PaO2) potential brain damage and death
define hypoxia
inadequate oxygen supply to tissues, various causes
5 causes of hypoxia
hypoxaemic anaemic stagnant histotoxic metabolic
hypoxaemic hypoxia
most common
reduced oxygen diffusion at the lungs
either due to reduced PO2 in the atmosphere OR tissue pathology
anaemic hypoxia
reduced oxygen carrying capacity of blood due to anaemia
stagnant hypoxia
heart disease
insufficient pumping ability of blood to lungs/around the body
histotoxic hypoxia
poisoning prevents cells using the oxygen delivered to them
e.g. CO, CN-
metabolic hypoxia
oxygen delivery to tissues doesnt meet increased oxygen demand by cells
carbon dioxide transport in the blood
7% dissolved in plasma and RBC
23% combined in RBC w/ deoxy Hb–> carbaminocompunds
70% combines in RBC w/ water (carbonic anhydrase) –> carbonic acid (dissociates into H+ and HCO3-)
most HCO3- moves out into plasma in exchange for Cl- (chloride shift)
XS H+ binds to Hb
CO2 movement in pulmonary capillaries
the reverse occurs in pulmonary capillaries and CO2 moves down its conc grad from blood to alveoli
acid-base balance
CO2 is capable of changing ECF pH
increased CO2 = reduced pH (increased H+)
How does CO2 change ECF pH
CO2 + H2O H2CO3 HCO3- + H+
why is pH normally stable
all the CO2 produced is eliminated in expired air
what alters plasma PCO2
hypo/hyperventilation
plasma [H+] will vary accordingly
hypoventilation and pH
CO2 retention
increased [H+]
respiratory acidosis
hyperventilation and pH
more CO2 blown off
reduced [H+]
respiratory alkalosis
